CTNND1 (Catenin Delta 1)

Endometrial factors can lead to infertility, but the exact molecules involved in endometrial receptivity remain unclear. Human endometrial receptivity is best assessed by determining whether a human blastocyst can attach and implant onto the endometrium of interest. With the use of a human embryo surrogate named BAP-EB, we demonstrated the important roles of CDH1 and CTNND1 in human embryo attachment. In particular, we showed that homophilic binding between trophectodermal CDH1 and epithelial CDH1 was one of the major mediators of the first contact in embryo-maternal interaction. Embryo-derived factors induced apical redistribution of CTNND1 and CDH1 in the EEC. Most importantly, the expression of CDH1 on the apical region of EEC represented endometrial receptivity. The results strengthen our understanding of embryo-maternal interaction in humans, and CDH1 could potentially be used for predicting IVF outcomes, which helps clinicians to better counsel the couples who fail with ART.

Biopsy of the right breast lesion confirmed a carcinoma histopathologically and immunohistochemically identical to that found in the eyelid biopsy. This case's histopathological features of invasive ductal breast carcinoma masquerading as invasive lobular carcinoma exemplify the challenging complexity of mixed disease.

Consequently, ZDHHC13 activity suppresses tumor growth and metastasis in immunocompetent mice. Our study highlights the therapeutic potential of targeting the ZDHHC13-E-cadherin axis and its downstream metabolic and immune-modulatory mechanisms, offering additional strategies to inhibit melanoma progression and metastasis.

Combination of PIMS and NPOT coupled to label-free quantitative proteomics point towards the distinct panitumumab mode of action in CRC patients and highlights specific proteins as prognostic biomarkers which need further validation in a bigger cohort and multicentric investigation, ideally involving patient registry follow up data.

These findings suggest that p120 may function to prevent the development or expression of depressive symptoms by suppressing proinflammatory NF-κB-IL-1β signaling in the hippocampus. Targeting p120 may be a feasible therapeutic strategy to treat MDD.

Finally, TCDD enhanced the motility and migration ability of prostate cancer cells through δ-catenin. These findings suggest that TCDD plays a role in stabilizing δ-catenin in prostate cancer cells, offering a new perspective on preventing δ-catenin degradation and potentially increasing the predictive value of δ-catenin for prostate cancer.

These changes correlate with decreased expression of cell adhesion molecules, suggesting a disruption of the mucosal barrier integrity. Consequently, SIAE-mediated sialic acid de-acetylation emerges as a critical factor in UC pathogenesis, potentially serving as both a valuable biomarker and a promising therapeutic target.

Through peritumoral injection, TTF-L-C enhanced tumor immunotherapy in both subcutaneous and recurrent 4T1 tumor models with satisfactory biosafety. Therefore, TTF-L-C is proposed to become a safe and powerful platform for various biomedical applications.

This review highlights recent progress in various aspects of ILC, including its unique molecular alteration, pathological classification and diagnostic approach, tumor biology and behavior, key clinical management challenges, and ongoing clinical trials, as well as the role of artificial intelligence in diagnosing ILC radiologically and pathologically. The goal of this review is to provide an updated understanding of the tumor biology, clinical manifestations, and molecular landscape of ILC and to help refine current tumor classification and diagnosis, subsequently improving management strategies and overall outcomes for lobular carcinoma patients.

The biogenesis of HCETSR and tRNA-Glu/TTC is regulated by the spliceosome and Dicer1. In conclusion, These findings suggest that HCETSR, derived from tRNA-Glu/TTC, inhibits HCC malignancy via modulation of the SPTBN1/catenin axis and may represent a promising prognostic marker and therapeutic strategy for HCC.

This triggers the dissociation of p120-catenin from the X-dimer cytoplasmic region, which increases P-cadherin turnover and targets the cadherin-antibody complex to the lysosome. Our results establish an outside-in signaling mechanism that provides fundamental insights into how cells regulate adhesion and that can be exploited by anti-cadherin antibodies for intracellular drug delivery.

In ILC, E-cadherin loss promotes hyperactivation of growth factor receptors, in particular insulin-like growth factor 1 receptor, anoikis resistance and synthetic lethality with ROS1 inhibition. These features introduce clinical vulnerabilities that could potentially be exploited to improve outcomes for ILC patients, for whom there are currently limited tailored treatments available.